The reticular thalamus (RT) is a thin shell of GABAergic neurons that provides a lateral border around the dorsal thalamus. Its axons synapse into primary thalamic relay nuclei supplying both feedforward and feedback inhibition from the cortex and thalamus respectively. The RT is topographically organized such that it primarily receives inputs of specific sensory modalities (e.g., vision, somatosensation, and audition) and can regulate the activity of the thalamic neurons within that same relay. In particular, the somatosensory RT has been implicated in the generation of absence seizures, brief periods of unconsciousness accompanied by a lapse in motor function. Interestingly, other RT regions have been linked to selective attention, an important feature of cognitive flexibility that is often disrupted in epileptic individuals. Under normal conditions, RT output suppresses incoming distracting information by selectively inhibiting thalamic subregions that represent information irrelevant in the current context for guiding appropriate behavior. Importantly, changes in top-down regulation of the RT can disrupt normal RT activation patterns and impair the sensory gating necessary for selective attention tasks. This suggests that changes in synaptic regulation of RT neurons can interrupt normal RT activity on which selective attention depends. Our lab has recently shown that in mice with disrupted expression of the voltage gated sodium channel, Nav1.6 (Scn8a+/-), reductions in somatosensory intra-RT synaptic inhibition lead to pathological thalamocortical (TC) oscillations and frequent absence seizures. We hypothesize that this same loss of intra-RT inhibition may occur broadly throughout the RT and lead to attentional deficits in the Scn8a+/- model of absence epilepsy. A loss of RT-RT inhibition would reduce local inhibition of RT cells, thus increasing overall RT activity, and decreasing the sensory throughput of inhibited thalamic neurons. Using a multi-level approach including behavior, circuit, and single-cell analysis we will address the fundamental question of whether there is widespread dysregulation of the RT in absence epilepsy. Further, our results will enable us to determine whether a common set of RT cells is responsible for both absence seizure generation and attentional impairments, highlighting shared mechanisms in both pathologies.